Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2005;46:29-30
Published online before print June 13, 2005, doi: 10.1161/01.HYP.0000171478.40560.3c
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
46/1/29    most recent
01.HYP.0000171478.40560.3cv1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnson, F. K.
Right arrow Articles by Durante, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnson, F. K.
Right arrow Articles by Durante, W.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*High Blood Pressure
Related Collections
Right arrow Animal models of human disease
Right arrow Pathophysiology
Right arrow Other hypertension
Right arrow Endothelium/vascular type/nitric oxide
Right arrowRelated Article

(Hypertension. 2005;46:29.)
© 2005 American Heart Association, Inc.


Editorial Commentaries

Aldosterone Promotes Endothelial Dysfunction Via Prostacyclin Independent of Hypertension

Fruzsina K. Johnson; Robert A. Johnson; William Durante

From the Tulane Hypertension and Renal Center of Excellence (F.K.J., R.A.J.), and Department of Physiology, Tulane University Health Sciences Center, New Orleans, La; and the Michael E. DeBakey VA Medical Center (W.D.), and Departments of Medicine and Pharmacology, Baylor College of Medicine, Houston, Tex.

Correspondence to Fruzsina K. Johnson, MD, Assistant Professor, Department of Physiology, Tulane University Health Sciences Center, 1430 Tulane Avenue, SL-39, New Orleans, LA 70112. E-mail Fruzsi123@aol.com


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

The renin-angiotensin-aldosterone system plays a key role in the regulation of blood pressure and water/electrolyte homeostasis. Classically, angiotensin II causes arteriolar vasoconstriction and increases aldosterone levels, whereas aldosterone promotes sodium and water reabsorption and potassium secretion via renal mineralocorticoid receptors. It is now well-accepted that inappropriate activation of the renin-angiotensin-aldosterone system not only increases blood pressure but also can play an important role in end-organ damage. Although Selye et al have demonstrated that administration of a mineralocorticoid combined with sodium promotes malignant hypertension and end-organ damage,1 subsequent clinical and experimental studies have focused on the pathological effects of angiotensin II, rather than aldosterone, and demonstrated that angiotensin-converting enzyme inhibitors, as well as angiotensin II receptor antagonists, confer significant cardiovascular protection.

Recent discoveries have revolutionized our view of aldosterone and its biological actions, and identified mineralocorticoids as important mediators of cardiovascular injury.2,3 The demonstration of rapid aldosterone effects challenged the exclusive role of mineralocorticoid receptor-mediated genomic actions in aldosterone signaling.4 Furthermore, it is now well-established that aldosterone can exert effects in nonepithelial and extrarenal tissues.2 Moreover, mineralocorticoids not only exert effects on extrarenal tissues but also can be synthesized outside the adrenal cortex.5 Aldosterone has now been shown to promote cardiovascular inflammation, endothelial dysfunction, and fibrosis.2 Furthermore, the effects of aldosterone can be independent of blood pressure, because mineralocorticoid receptor blockade can confer cardiovascular protection without lowering the blood pressure.6 In the light of these advancements, recent clinical trials have shown the cardiovascular protective benefits of mineralocorticoid receptor blockade.7

In this . . . [Full Text of this Article]


Related Article:

Participation of Prostacyclin in Endothelial Dysfunction Induced by Aldosterone in Normotensive and Hypertensive Rats
Javier Blanco-Rivero, Victoria Cachofeiro, Vicente Lahera, Rosa Aras-Lopez, Iván Márquez-Rodas, Mercedes Salaices, Fabiano E. Xavier, Mercedes Ferrer, and Gloria Balfagón
Hypertension 2005 46: 107-112. [Abstract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
G. Lastra, A. Whaley-Connell, C. Manrique, J. Habibi, A. A. Gutweiler, L. Appesh, M. R. Hayden, Y. Wei, C. Ferrario, and J. R. Sowers
Low-dose spironolactone reduces reactive oxygen species generation and improves insulin-stimulated glucose transport in skeletal muscle in the TG(mRen2)27 rat
Am J Physiol Endocrinol Metab, July 1, 2008; 295(1): E110 - E116.
[Abstract] [Full Text] [PDF]


Home page
Diabetes CareHome page
J. L. Kitzmiller, L. Dang-Kilduff, and M. M. Taslimi
Gestational Diabetes After Delivery: Short-term management and long-term risks
Diabetes Care, July 1, 2007; 30(Supplement_2): S225 - S235.
[Full Text] [PDF]